OCULAR FLUID COMPOSITION AND OCULAR TISSUE PHYSIOLOGY

这是一个综合计划的延续，旨在阐明 正常眼内液成分和眼压的动态平衡机制 房水动力学和确定房水改变的作用 眼内微环境--由于病理生理或 血管通透性和转运功能的病理变化 血-眼屏障--(年龄相关的)眼部病理。我们会 继续我们之前开始的一些工作(例如 前列腺素和眼内稳态中的其他转运过程)，但我们 将专注于测试和阐明一组 假说是在那段时间里提出的。这些假设，大部分 这与我们的进化分化假说直接相关 眼睛防御机制，陈述或暗示以下内容：在一些 物种，尤其是兔子，破坏血-房水屏障(BAB) 代表了一种复杂的(自体激素调节的)递送机制 用于角膜修复的凝血因子(以及可能的其他)； 依赖高视觉敏锐度的物种，Bab崩溃的发生较少 很容易，但纤维蛋白原和其他蛋白质可以进入前房 通过角膜穿透后的小管反流；有效的宝贝 破裂和小管反流取决于前葡萄膜和瓣膜周围 分别为充血；刺激引起的充血 这些站点由类似的机制调节，并且可能由相同的 眼内炎症的那段插曲(S)可以引起 血液运输性质的长期或永久性变化 眼屏障，因此在眼内微环境中，从而 导致慢性单纯性青光眼、老花眼、 老年性白内障与黄斑囊样水肿。 更好地了解眼睛刺激和炎症反应以及 这些反应中的物种差异不仅会让理性的 选择适用于人类眼病的动物模型，但将 促进对这些疾病的外科和治疗方法的发展 疾病和这些方法在兽医中的适应 眼科。更好地理解这种反应的机制 鉴于日益增长的需求，显然需要对它们进行控制 复杂和积极的方法来延长有用的视觉期 在日益长寿的人口中。

This is a continuation of an integrated program designed to elucidate the mechanisms of the homeostasis of normal intraocular fluid composition and aqueous humor dynamics and to determine the role of alterations in intraocular micro-environments - as a result of pathophysiological or pathological changes in the permeability and transport functions of the blood-ocular barriers - in (age-dependent) ocular pathologies. We will continue some of our work initiated previously (such as the role of Prostaglandin and other transport processes in ocular homeostasis), but we will focus on testing and elucidating the implications of a set of hypotheses developed during that grant period. These hypotheses, most of which directly relate to our hypothesis of evolutionary divergence in ocular defense mechanisms, state or imply the following: that in some species, especially rabbits, breakdown of the blood acueous barrier (BAB) represents a sophisticated (autocoid mediated) mechanism for the delivery of clotting (and possibly other) factors for corneal repair; that in species which depend on high visual acuity, BAB breakdown occurs less readily, but fibrinogen and other proteins can enter the anterior chamber by canalicular reflux after corneal penetration; that effective BAB breakdown and canalicular reflux depend on anterior uveal and perilimbal hyperemia, respectively; that irritation-induced hyperemia at either of these sites is mediated by a similar mechanism, and possibly by the same autacoids; that episode(s) of intraocular inflammation can cause long-lasting or permanent changes in the transport properties of the blood ocular barrier and, hence, in the intraocular microenvironment, thereby contributing to such disorders as chronic simple glaucoma, presbyopia, senile cataracts and cystoid macular edema. A better understanding of ocular irritative and inflammatory responses and of species differences in these responses will not only allow the rational selection of applicable animal models for human ocular disorders, but will facilitate the development of surgical and therapeutic approaches to these disorders and the adaptation of these approaches to veterinary ophthalmology. A better understanding of the mechanisms of such responses and their control is clearly required in view of the need for increasingly sophisticated and aggressive means of extending the period of useful vision in an increasingly longevous population.